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Objective To explore correlation between serum bilirubin and sleep disorders in Parkinson's disease (PD) patients. Methods Total 79 PD cases from He'nan Provincial People's Hospital, and 77 age and sex matched controls were recruited from October 2021 to October 2022. The Unified Parkinson Disease Rating Scale III (UPDRS III) was used to evaluate motor symptoms, modified Hoehn-Yahr staging was used to evaluate disease severity, Rapid Eye Movement Sleep Behavior Disorder Questionnaire-Hong Kong (RBDQ-HK) was used to access the severity of rapid eye movement sleep behavior disorder (RBD), Pittsburgh Sleep Quality Index (PSQI) was used to access the sleep quality, and Epworth Sleepiness Scale (ESS) was used to access the occurrence of excessive daytime sleepiness (EDS). The levels of serum total bilirubin (TBIL), indirect bilirubin (IBIL) and direct bilirubin (DBIL) were measured. Results Seventy-nine PD patients were divided into the early PD group (n = 47) and middle-late PD group (n = 32). The levels of TBIL (Z = 4.988, P = 0.000; Z = 3.917, P = 0.000), IBIL (Z = 4.860, P = 0.000; Z = 3.827, P = 0.000) and DBIL (Z = 4.054, P = 0.000; Z = 3.468, P = 0.002) in the early PD group and middle-late PD group were lower than those in the control group. Correlation analysis showed serum TBIL levels were negatively correlated with PSQI score (r = - 0.310, P = 0.006) and ESS score (r = -0.254, P =0.027), serum IBIL levels were negatively correlated with PSQI score (r = - 0.284, P = 0.013), serum DBIL levels were negatively correlated with RBDQ-HK score (r =-0.244, P = 0.034), PSQI score (r = - 0.288, P = 0.012) and ESS score (r = - 0.295, P = 0.010). Conclusions Serum bilirubin in PD patients were lower than those in the control group inferring that a decrease in serum bilirubin might be a potential mechanism for the occurrence of PD. The lower serum bilirubin was, the more severe sleep disorders in PD patients were. [ABSTRACT FROM AUTHOR]

Abstract Background Recently, the anti-tumor activity of N-myc downstream-regulated gene 2 (NDRG2) was shown decreased expression in clear cell renal cell carcinoma (CCRCC), but the role of the down-expression of NDRG2 has not been described. Methods The NDRG2 recombinant adenovirus plasmid was constructed. The proliferation rate and NDRG2 expression of cell infected with recombinant plasmid were mesured by MTT, Flow cytometry analysis and western blot. Results The CCRCC cell A-498 re-expressed NDRG2 when infected by NDRG2 recombinant adenovirus and significantly decreased the proliferation rate. Fluorescence activated cell sorter analysis showed that 25.00% of cells expressed NDRG2 were in S-phase compared to 40.67% of control cells, whereas 62.08% of cells expressed NDRG2 were in G1-phase compared to 54.39% of control cells (P < 0.05). In addition, there were much more apoptotic cells in NDRG2-expressing cells than in the controls (P < 0.05). Moreover, upregulation of NDRG2 protein was associated with a reduction in cyclin D1, cyclin E, whereas cyclinD2, cyclinD3 and cdk2 were not affected examined by western blot. Furthermore, we found that p53 could upregulate NDRG2 expression in A-498 cell. Conclusions We found that NDRG2 can inhibit the proliferation of the renal carcinoma cells and induce arrest at G1 phase. p53 can up-regulate the expression of NDRG2. Our results showed that NDRG2 may function as a tumor suppressor in CCRCC.